The aim of this study was to examine (a) whether adventurous and explosive temperament profiles (presumed precursors of antisocial and borderline personality) are associated with character traits over a 15-year follow-up and (b) whether social support and attachment security modify the relationship between temperament profiles and character development.
2,028 subjects of the Young Finns study completed the Temperament and Character Inventory, the Multidimensional Scale of Perceived Social Support, and the Relationship Questionnaire at 3 assessment points between 1997 and 2012.
Both explosive and adventurous temperament profiles seemed to predispose individuals to have less mature personalities; that is, these profiles were consistently associated with lower cooperativeness (P
Lp(a) (lipoprotein(a)) concentrations are widely genetically determined by the LPA isoforms and show 5-fold interpopulation differences. Two- to 3-fold differences have been reported even within Europe. Finns represent a distinctive population isolate within Europe and have been repeatedly reported to present lower Lp(a) concentrations than Central Europeans. The significance of this finding was unclear for a long time because of the difficult comparability of Lp(a) assays. Recently, a large standardized study in >50?000 individuals from 7 European populations confirmed this observation but could not provide insights into the causes.
We investigated Lp(a) concentrations, LPA isoforms, and genotypes of established genetic variants affecting Lp(a) concentrations (LPA variants, APOE isoforms, and PCSK9 R46L) in the Finnish YFS (Cardiovascular Risk in Young Finns Study) population (n=2281) and 3 Non-Finnish Central European populations (n=10?003). We observed ˜50% lower Lp(a) concentrations in Finns. The isoform distribution was shifted toward longer isoforms, and the percentage of low-molecular-weight isoform carriers was reduced. Most interestingly, however, Lp(a) was reduced in each single-isoform group. In contrast to the known inverse relationship between LPA isoforms and Lp(a) concentrations, especially very short isoforms presented unexpectedly low Lp(a) concentrations in Finns. The investigated genetic variants, as well as age, sex, and renal function, explained 71.8% of the observed population differences.
The population differences in Lp(a) concentrations between Finnish and Central European populations originate not only from a different LPA isoform distribution but suggest the existence of novel functional variation in the small-isoform range.
The aim of this study was to investigate (i) the direction of the relationships between dispositional compassion for others and depressive symptoms over a 15-year follow-up in adulthood and (ii) the longitudinal associations of dispositional compassion with total depressive symptoms and various depressive subsymptoms (i.e. negative attitude, performance difficulties, and somatic complaints) from early adulthood to middle age.
The participants (N?=?1676) came from the prospective Young Finns Study. Dispositional compassion was assessed with the Temperament and Character Inventory and depressive symptoms with a modified version of the Beck Depression Inventory. The measurements were conducted between 1997-2012 including three measurement points. The data was analyzed using structural equation models and multilevel models for longitudinal design.
The predictive relationships were more likely to proceed from high dispositional compassion for others to lower depressive symptoms than in the opposite direction. Additionally, high dispositional compassion predicted a lower total score of depressive symptoms and also lower scores of various depressive subsymptoms (negative attitude, performance difficulties, somatic complaints) in early adulthood. These associations, however, weakened over years and became non-significant in middle age. All the findings were sustained after controlling for age, gender, and socioeconomic factors in childhood and adulthood.
Depressive symptoms were mostly mild and non-clinical in our sample. The findings cannot be directly generalized to severe depressive symptomatology.
When tailoring psychiatric interventions, it is necessary to be aware that compassion for others may lower the risk for the onset and maintenance of depressive symptoms, especially in early adulthood.
To determine whether vitamin D status in childhood and adolescence (herein collectively referred to as youth) and the long-term status from youth to adulthood is associated with risk of developing type 2 diabetes mellitus (T2DM) and impaired fasting glucose (IFG) in adulthood.
This was a 31-year follow-up study of 2300 participants aged 3-18 years. Multinomial logistic regression was used to assess the association of both (a) baseline 25-hydroxyvitamin D (25OHD) levels and (b) the mean of baseline and the latest follow-up 25OHD levels (continuous variable and quartiles) with incident T2DM and IFG (cut-off?=?5.6?mmol/L) in adult life.
High serum 25OHD levels in youth and also mean values from youth to adulthood were associated with reduced risk of developing T2DM in adulthood (odds ratio, 95% confidence interval=?0.73, 0.57-0.95 and 0.65, 0.51-0.84, respectively, for each SD increment in 25OHD). Compared to Q1, a dose-dependent negative association was observed across other quartiles of youth 25OHD, while the strongest association was found in the Q3 for the mean 25OHD levels. Neither youth nor the mean 25OHD was associated with IFG.
High serum 25OHD levels in youth, and from child to adult life, were associated with a reduced risk of developing T2DM in adulthood. Key Messages High serum 25OHD levels in youth, and between youth and adulthood, were associated with a lower risk of T2DM in adulthood. Each SD (15.2?nmol/L) increment in youth serum 25OHD levels was associated with a 26% reduction in odds for T2DM, which was independent of a number of confounding variables and other risk factors for T2DM. A similar magnitude of association was observed for the long-term 25OHD levels between youth and adulthood. These findings suggest a potentially simple and cost-effective strategy for reducing adulthood risk of T2DM starting in an earlier stage of life - improving and maintaining vitamin D status throughout youth and early adulthood.
Using participants (N?=?1733) drawn from the nationally representative longitudinal Young Finns Study (YFS) we estimate the effect of education on depressive symptoms. In 2007, when the participants were between 30 and 45?years old, they reported their depressive symptoms using a revised version of Beck's Depression Inventory. Education was measured using register information on the highest completed level of education in 2007, which was converted to years of education. To identify a causal relationship between education and depressive symptoms we use an instrumental variables approach (Mendelian randomization, MR) with a genetic risk score as an instrument for years of education. The genetic risk score was based on 74 genetic variants, which were associated with years of education in a genome-wide association study (GWAS). Because the genetic variants are randomly assigned at conception, they induce exogenous variation in years of education and thus identify a causal effect if the assumptions of the MR approach are met. In Ordinary Least Squares (OLS) estimation years of education in 2007 were negatively associated with depressive symptoms in 2007 (b?=?-0.027, 95% Confidence Interval (CI)?=?-0.040, -0.015). However, the results based on Mendelian randomization suggested that the effect is not causal (b?=?0.017; 95% CI?=?-0.144, 0.178). This indicates that omitted variables correlated with education and depression may bias the linear regression coefficients and exogenous variation in education caused by differences in genetic make-up does not seem to protect against depressive symptoms.
Aortic sinus dilatation can lead to aortic valve regurgitation or even aortic dissection. Our objective was to examine the association between body surface area (BSA) measures from childhood to middle age and aortic sinus diameter in middle age. Understanding the relation of these two clarifies how aortic size is normally determined.
Cardiovascular Risk in Young Finns Study is a longitudinal study with follow-up of over 31 years (1980-2011). The study comprises information of body composition from multiple time points of 1950 subjects with cardiac ultrasound measurements made in 2011. The association between BSA in different ages and aortic sinus diameter in middle age was analysed by linear regression modelling adjusted with age, sex and diastolic blood pressure. Missing BSA values were derived for each life year (ages 3-33 years) from subject-specific curves for body weight and height estimated from longitudinal measurements using mixed model regression splines.
BSA estimates in early 20s are most strongly associated with aortic sinus diameter in middle age. Top association was observed at age 23 years with one SD increase in estimated BSA corresponding to 1.04?mm (0.87-1.21?mm) increase in aortic diameter. Increase in body weight beyond early 20s does not associate with aortic sinus diameter, and the association between middle age BSA and aortic size is substantially weaker (0.74?mm increase (0.58-0.89?mm)). These results were confirmed in a subpopulation using only measured data.
The association between aortic sinus diameter and BSA is stronger when considering BSA in young adulthood compared with BSA in middle age.
The aim of this study was to examine (a) the associations of temperament and character dimensions with paranoid ideation over a 15-year follow-up in the general population (b) the associations of explosive temperament and organized character profiles with paranoid ideation. 2137 subjects of the Young Finns Study completed the Temperament and Character Inventory and the Paranoid Ideation Scale of the Symptom Checklist-90 Revised in 1997, 2001, and 2012. Temperament dimensions of high novelty seeking, high harm avoidance, low reward dependence and explosive temperament profile were associated with the development of higher paranoid ideation. Regarding character, high self-directedness, high cooperativeness, and low self-transcendence and organized character profile were associated with lower paranoid ideation. These associations sustained after controlling for age, gender, and socioeconomic factors. However, the associations between temperament and paranoia mostly disappeared after taking character into account. Our study supported the hypothesis that personality dimensions contribute to the development of paranoid ideation. Temperament and character might combine a variety of single previously found risk factors into a more comprehensive framework for the developmental etiology of paranoia. Our findings provide evidence for psychotherapeutic interventions that support the self-regulation of temperamental vulnerabilities by internalizing mature concepts about the self and social relationships.
The aim of this study was to examine longitudinally in the general population (a) whether depressive symptoms co-occur with paranoid ideation from late adolescence to middle age (b) whether depressive subsymptoms are differently linked with paranoid ideation (c) whether depressive symptoms are associated with state-level or trait-level paranoid ideation.
Altogether 2109 subjects of the Young Finns study completed the Paranoid Ideation Scale of the Symptom Checklist-90 Revised and a modified version of the Beck Depression Inventory in 1992, 1997, 2001, 2007, and 2012, and the Beck Depression Inventory-II in 2007, 2011, and 2012.
Higher self-rated depressive symptoms were associated with the course of more severe paranoid ideation over age, especially in late adolescence and early adulthood. Regarding depressive subsymptoms, the associations of negative attitude and performance difficulties with paranoid ideation were evident over age, whereas the influence of somatic symptoms (such as changes in sleep and appetite) was not significant until after early adulthood. Additionally, depressive symptoms were more evidently associated with the development of trait- than state-level paranoid ideation.
Our study mostly captured mild depressive and paranoid symptoms. The results cannot be directly generalized to clinical populations.
Depressive symptoms were associated with the course of paranoid ideation from late adolescence to middle age. Patients with paranoid ideation might merit from evaluation of potential depressive symptoms, especially in late adolescence and early adulthood. Among patients with co-occurring depressive symptoms and paranoid ideation, there may be a substantial need for neurocognitive rehabilitation and community-based treatments.
Type 2 diabetes (T2D) has been associated with depressive symptoms, but the causal direction of this association and the underlying mechanisms, such as increased glucose levels, remain unclear. We used instrumental-variable regression with a genetic instrument (Mendelian randomization) to examine a causal role of increased glucose concentrations in the development of depressive symptoms.
Data were from the population-based Cardiovascular Risk in Young Finns Study (n = 1217). Depressive symptoms were assessed in 2012 using a modified Beck Depression Inventory (BDI-I). Fasting glucose was measured concurrently with depressive symptoms. A genetic risk score for fasting glucose (with 35 single nucleotide polymorphisms) was used as an instrumental variable for glucose.
Glucose was not associated with depressive symptoms in the standard linear regression (B = -0.04, 95% CI [-0.12, 0.04], p = .34), but the instrumental-variable regression showed an inverse association between glucose and depressive symptoms (B = -0.43, 95% CI [-0.79, -0.07], p = .020). The difference between the estimates of standard linear regression and instrumental-variable regression was significant (p = .026) CONCLUSION: Our results suggest that the association between T2D and depressive symptoms is unlikely to be caused by increased glucose concentrations. It seems possible that T2D might be linked to depressive symptoms due to low glucose levels.
Cites: BMJ. 2005 Mar 26;330(7493):705-6 PMID 15684022
Cites: Int J Epidemiol. 2008 Dec;37(6):1220-6 PMID 18263651
Cites: BMJ. 2003 Dec 13;327(7428):1383-4 PMID 14670883
MicroRNAs are involved in disease development and may be utilized as biomarkers. We investigated the association of blood miRNA levels and a) fatty liver (FL), b) lipoprotein and lipid pathways involved in liver lipid accumulation and c) levels of predicted mRNA targets in general population based cohort. Blood microRNA profiling (TaqMan OpenArray), genome-wide gene expression arrays and nuclear magnetic resonance metabolomics were performed for Young Finns Study participants aged 34-49 years (n?=?871). Liver fat status was assessed ultrasonographically. Levels of hsa-miR-122-5p and -885-5p were up-regulated in individuals with FL (fold change (FC)?=?1.55, p?=?1.36?*?10-14 and FC?=?1.25, p?=?4.86?*?10-4, respectively). In regression model adjusted with age, sex and BMI, hsa-miR-122-5p and -885-5p predicted FL (OR?=?2.07, p?=?1.29?*?10-8 and OR?=?1.41, p?=?0.002, respectively). Together hsa-miR-122-5p and -885-5p slightly improved the detection of FL beyond established risk factors. These miRNAs may be associated with FL formation through the regulation of lipoprotein metabolism as hsa-miR-122-5p levels associated with small VLDL, IDL, and large LDL lipoprotein subclass components, while hsa-miR-885-5p levels associated inversely with XL HDL cholesterol levels. Hsa-miR-885-5p levels correlated inversely with oxysterol-binding protein 2 (OSBPL2) expression (r?=?-0.143, p?=?1.00?*?10-4) and suppressing the expression of this lipid receptor and sterol transporter could link hsa-miR-885-5p with HDL cholesterol levels.
Prediabetes often occurs together with dyslipidaemia, which is paradoxically treated with statins predisposing to type 2 diabetes mellitus. We examined peripheral blood pathway profiles in prediabetic subjects with (PRD ) and without dyslipidaemia (PR0 ) and compared these to nonprediabetic controls without dyslipidaemia (C0 ).
The participants were from the Cardiovascular Risk in Young Finns Study, including 1240 subjects aged 34 to 49 years. Genome-wide expression data of peripheral blood and gene set enrichment analysis were used to investigate the differentially expressed genes and enriched pathways between different subtypes of prediabetes.
Pathways for cholesterol synthesis, interleukin-12-mediated signalling events, and downstream signalling in naïve CD8+ T-cells were upregulated in the PR0 group in comparison with controls (C0 ). The upregulation of these pathways was independent of waist circumference, blood pressure, smoking status, and insulin. Adjustment for CRP left the CD8+ T-cell signalling and interleukin-12-mediated signalling event pathway upregulated. The cholesterol synthesis pathway was also upregulated when all prediabetic subjects (PR0 and PRD ) were compared with the nonprediabetic control group. No pathways were upregulated or downregulated when the PRD group was compared with the C0 group. Five genes in the PR0 group and 1 in the PRD group were significantly differentially expressed in comparison with the C0 group.
Blood cell gene expression profiles differ significantly between prediabetic subjects with and without dyslipidaemia. Whether this classification may be used in detection of prediabetic individuals at a high risk of cardiovascular complications remains to be examined.
More education is associated with a lower body mass index (BMI) and likelihood of being overweight. However, since a large proportion of the variation in body mass is due to genetic makeup, it has been hypothesized that education may moderate the genetic risk. We estimate main associations between (i) education, (ii) genetic risk, and (iii) interactions between education and genetic risk on BMI and the probability of being overweight in the UK and Finland. The estimates show that education is negatively associated with BMI and overweightness, and genetic risk is positively associated. However, the interactions between education and genetic risk are small and statistically insignificant.
The aim of this explorative study was to examine the effect of education on obesity using Mendelian randomization.
Participants (N=2011) were from the on-going nationally representative Young Finns Study (YFS) that began in 1980 when six cohorts (aged 30, 33, 36, 39, 42 and 45 in 2007) were recruited. The average value of BMI (kg/m2) measurements in 2007 and 2011 and genetic information were linked to comprehensive register-based information on the years of education in 2007. We first used a linear regression (Ordinary Least Squares, OLS) to estimate the relationship between education and BMI. To identify a causal relationship, we exploited Mendelian randomization and used a genetic score as an instrument for education. The genetic score was based on 74 genetic variants that genome-wide association studies (GWASs) have found to be associated with the years of education. Because the genotypes are randomly assigned at conception, the instrument causes exogenous variation in the years of education and thus enables identification of causal effects.
The years of education in 2007 were associated with lower BMI in 2007/2011 (regression coefficient (b)=-0.22; 95% Confidence Intervals [CI]=-0.29, -0.14) according to the linear regression results. The results based on Mendelian randomization suggests that there may be a negative causal effect of education on BMI (b=-0.84; 95% CI=-1.77, 0.09).
The findings indicate that education could be a protective factor against obesity in advanced countries.
This paper uses longitudinal survey data linked to administrative registers to examine socioeconomic gradients in health, particularly whether the effects of genetic endowments interact with the socioeconomic resources of the parental household. We find that genetic risk scores contribute to adult health measured by biomarkers. This result is consistent with the findings from genome-wide association studies. Socioeconomic gradients in health differ based on biomarker and resource measures. Family education is negatively related to obesity and the waist-hip ratio, and family income is negatively related to low-density lipoprotein cholesterol and triglyceride levels. Parental resources do not modify the effects of genetic endowment on adult health. However, there is evidence for gene-family income interactions for triglyceride levels, particularly among women.
Fatty liver is a potentially preventable cause of serious liver diseases. This longitudinal study aimed to identify childhood risk factors of fatty liver in adulthood in a population-based group of Finnish adults.
Study cohort included 2,042 individuals from the Cardiovascular Risk in Young Finns Study aged 3-18years at baseline in 1980. During the latest follow-up in 2011, the liver was scanned by ultrasound. In addition to physical and environmental factors related to fatty liver, we examined whether the genetic risk posed by a single nucleotide polymorphism in the patatin-like phospholipase domain-containing protein 3 gene (PNPLA3) (rs738409) strengthens prediction of adult fatty liver.
Independent childhood predictors of adult fatty liver were small for gestational age, (odds ratio=1.71, 95% confidence interval=1.07-2.72), variant in PNPLA3 (1.63, 1.29-2.07 per one risk allele), variant in the transmembrane 6 superfamily 2 gene (TM6SF2) (1.57, 1.08-2.30), BMI (1.30, 1.07-1.59 per standard deviation) and insulin (1.25, 1.05-1.49 per standard deviation). Childhood blood pressure, physical activity, C-reactive protein, smoking, serum lipid levels or parental lifestyle factors did not predict fatty liver. Risk assessment based on childhood age, sex, BMI, insulin levels, birth weight, TM6SF2 and PNPLA3 was superior in predicting fatty liver compared with the approach using only age, sex, BMI and insulin levels (C statistics, 0.725 vs. 0.749; p=0.002).
Childhood risk factors on the development of fatty liver were small for gestational age, high insulin and high BMI. Prediction of adult fatty liver was enhanced by taking into account genetic variants in PNPLA3 and TM6SF2 genes.
The increase in pediatric obesity emphasizes the importance of identification of children and adolescents at high risk of fatty liver in adulthood. We used data from the longitudinal Cardiovascular Risk in Young Finns Study to examine the associations of childhood (3-18years) risk variables with fatty liver assessed in adulthood at the age of 34-49years. The findings suggest that a multifactorial approach with both lifestyle and genetic factors included would improve early identification of children with a high risk of adult fatty liver.
Helsinki Collegium for Advanced Studies, University of Helsinki, Helsinki, Finland; Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland. Electronic address: email@example.com.
Type 2 diabetes is a public health concern, but psychosocial factors that may protect against the disease are unknown. This study examines whether a positive psychosocial environment in childhood is associated with lower risk for Type 2 diabetes in adulthood or healthier glucose trajectories over the life course, and whether BMI mediates the associations.
A cohort of 3,596 Finnish children was followed into adulthood over 32 years. An overall positive psychosocial score, consisting of six subdomains, was measured at study baseline (1980). Relative risk ratios and multilevel growth curve modeling were used to examine associations of the psychosocial score with Type 2 diabetes (2012) and glucose trajectories (1986-2012). The mediating effect by BMI was examined using mediation analysis. The analyses were conducted between June 2015 and January 2016.
There was a 21% decrease in the rate of Type 2 diabetes (relative risk ratio, 0.79; 95% CI=0.66, 0.94) for each 1-SD increase in the positive psychosocial score after adjustment for childhood cardiovascular risk factors and dietary behaviors. Adult BMI mediated 52% and weight gain mediated 25% of the association. The growth curve model showed healthier glucose trajectories (age X psychosocial score interaction, b= -0.01; p=0.010) for participants with higher versus lower positive psychosocial score in childhood.
Positive psychosocial environment in childhood seems to have beneficial influences on the risk for Type 2 diabetes over the life span. RCTs will be required to see if interventions directed at early-life circumstances are warranted.
Neighbourhood characteristics have been associated with health behaviours of residents. We used longitudinal data to examine whether neighbourhood characteristics (level of urbanization and socioeconomic status) are related to within-individual variations in health behaviours (alcohol consumption, smoking, exercise and self-interest in health) as people live in different neighbourhoods over time.
Participants were from the Young Finns prospective cohort study (N = 3145) with four repeated measurement times (1992, 2001, 2007 and 2011/2012). Neighbourhood socioeconomic status and level of urbanization were measured on the level of municipality and zip code area. Within-individual (i.e. fixed-effect) regression was used to examine whether these associations were observed within individuals who lived in different neighbourhood in different measurement times.
People living in more urban zip code areas were more likely to smoke (b = 0.06; CI = 0.03-0.09) and drink alcohol (b = 0.11; CI = 0.08-0.14), and these associations were replicated in within-individual analysis-supporting social causation. Neighbourhood socioeconomic status and urbanization were associated with higher interest in maintaining personal health (b = 0.05; CI = 0.03-0.08 and b = 0.05; CI = 0.02-0.07, respectively), and these associations were also similar in within-individual analysis. Physical exercise was not associated with neighbourhood characteristics.
These data lend partial support for the hypothesis that neighbourhood differences influence people's health behaviours.
Hormonal contraception is commonly used worldwide, but its systemic effects across lipoprotein subclasses, fatty acids, circulating metabolites and cytokines remain poorly understood.
A comprehensive molecular profile (75 metabolic measures and 37 cytokines) was measured for up to 5841 women (age range 24-49 years) from three population-based cohorts. Women using combined oral contraceptive pills (COCPs) or progestin-only contraceptives (POCs) were compared with those who did not use hormonal contraception. Metabolomics profiles were reassessed for 869 women after 6 years to uncover the metabolic effects of starting, stopping and persistently using hormonal contraception.
The comprehensive molecular profiling allowed multiple new findings on the metabolic associations with the use of COCPs. They were positively associated with lipoprotein subclasses, including all high-density lipoprotein (HDL) subclasses. The associations with fatty acids and amino acids were strong and variable in direction. COCP use was negatively associated with albumin and positively associated with creatinine and inflammatory markers, including glycoprotein acetyls and several growth factors and interleukins. Our findings also confirmed previous results e.g. for increased circulating triglycerides and HDL cholesterol. Starting COCPs caused similar metabolic changes to those observed cross-sectionally: the changes were maintained in consistent users and normalized in those who stopped using. In contrast, POCs were only weakly associated with metabolic and inflammatory markers. Results were consistent across all cohorts and for different COCP preparations and different types of POC delivery.
Use of COCPs causes widespread metabolic and inflammatory effects. However, persistent use does not appear to accumulate the effects over time and the metabolic perturbations are reversed upon discontinuation. POCs have little effect on systemic metabolism and inflammation.
High alcohol consumption is a major cause of morbidity, yet alcohol is associated with both favourable and adverse effects on cardiometabolic risk markers. We aimed to characterize the associations of usual alcohol consumption with a comprehensive systemic metabolite profile in young adults.
Cross-sectional associations of alcohol intake with 86 metabolic measures were assessed for 9778 individuals from three population-based cohorts from Finland (age 24-45 years, 52% women). Metabolic changes associated with change in alcohol intake during 6-year follow-up were further examined for 1466 individuals. Alcohol intake was assessed by questionnaires. Circulating lipids, fatty acids and metabolites were quantified by high-throughput nuclear magnetic resonance metabolomics and biochemical assays.
Increased alcohol intake was associated with cardiometabolic risk markers across multiple metabolic pathways, including higher lipid concentrations in HDL subclasses and smaller LDL particle size, increased proportions of monounsaturated fatty acids and decreased proportion of omega-6 fatty acids, lower concentrations of glutamine and citrate (P?
Lower birthweight is associated with increased susceptibility to cardiometabolic diseases in adulthood, but the underlying molecular pathways are incompletely understood. We examined associations of birthweight with a comprehensive metabolic profile measured in adolescents and adults.
High-throughput nuclear magnetic resonance metabolomics and biochemical assays were used to quantify 87 circulating metabolic measures in seven cohorts from Finland and the UK, comprising altogether 18 288 individuals (mean age 26 years, range 15-75). Metabolic associations with birthweight were assessed by linear regression models adjusted for sex, gestational age and age at blood sampling. The metabolic associations with birthweight were compared with the corresponding associations with adult body mass index (BMI).
Lower birthweight adjusted for gestational age was adversely associated with cardiometabolic biomarkers, including lipoprotein subclasses, fatty acids, amino acids and markers of inflammation and impaired liver function (P
Cites: BMJ. 1989 Mar 4;298(6673):564-7 PMID 2495113
Cites: Int J Epidemiol. 2013 Feb;42(1):111-27 PMID 22507743